Bohnenberger, Hanibal

[["dc.bibliographiccitation.artnumber","e85"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","International Journal of Surgery. Oncology"],["dc.bibliographiccitation.lastpage","5"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Saha, Shekhar"],["dc.contributor.author","Yao, Sha"],["dc.contributor.author","Elakad, Omar"],["dc.contributor.author","Lois, Anna-Maria"],["dc.contributor.author","Henric-Petri, Hannah"],["dc.contributor.author","Buentzel, Judith"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Emmert, Alexander"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.date.accessioned","2020-06-09T11:55:48Z"],["dc.date.accessioned","2021-10-27T13:22:15Z"],["dc.date.available","2020-06-09T11:55:48Z"],["dc.date.available","2021-10-27T13:22:15Z"],["dc.date.issued","2020"],["dc.description.abstract","Background: UDP-glucose-6-dehydrogenase (UGDH) plays an important role in the production of hyaluronic acid, an extracellular matrix component that is responsible for the promotion of normal cellular growth and migration. Increased levels of UGDH have been linked to the progression of epithelial cancers, such as those of the breast, colon and prostate. Therefore we aimed to analyze if the expression level of UGDH does also influence patients survival of lung cancer patients. Methods: UGDH expression levels were analyzed by immunohistochemistry in 96 samples of pulmonary adenocarcinoma (AC), 84 cases of squamous cell lung carcinoma (SQCLC) and 33 samples of small cell lung cancer (SCLC) and correlated with clinicopathologic characteristics and patient outcome. Results: UGDH was expressed in 62.5% cases of AC, 70.2% cases of SQCLC, and 48.5% cases of SCLC. In AC, expression of UGDH was significantly associated with lymph node metastasis and worse overall survival of the affected patients. However, UGDH expression had no significant correlation to prognosis in SQCLC or SCLC patients. Conclusions: In our study, expression of UGDH was associated with worse prognosis of patients with pulmonary adenocarcinoma so that expression of UGDH might help to guide treatment decisions. Furthermore, UGDH might present a potential novel drug target in AC as it displays inhibitable catalytic activity."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2020"],["dc.identifier.doi","10.1097/IJ9.0000000000000085"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17377"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92078"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2471-3864"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","UDP-glucose 6-dehydrogenase expression as a predictor of survival in patients with pulmonary adenocarcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15437"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","15450"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Baake, Tina"],["dc.contributor.author","Jörß, Katharina"],["dc.contributor.author","Suennemann, Jennifer"],["dc.contributor.author","Roßmann, Laura"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2019-07-09T11:45:14Z"],["dc.date.available","2019-07-09T11:45:14Z"],["dc.date.issued","2018"],["dc.description.abstract","Graft-versus-host disease (GvHD) is a life-threatening complication of hematopoietic stem cell transplantation (HSCT), which is caused by allogeneic T cells recognizing molecules of the recipient as foreign. Endogenous glucocorticoids (GC) released from the adrenal gland are crucial in regulating such inflammatory diseases. Here we demonstrate that genetically engineered mice, that are largely unresponsive to GC, suffer from aggravated clinical symptoms and increased mortality after HSCT, effects that could be tempered by neutralization of IL-6. Interestingly, selective ablation of the GC receptor (GR) in recipient myeloid cells resulted in fulminant disease as well. While histopathological analysis of the jejunum failed to reveal any differences between sick mice of both genotypes, systemic IL-6 and TNFα secretion was strongly increased in transplanted mice lacking the GR in myeloid cells briefly before the majority of them succumbed to the disease. Collectively, our findings reveal an important role of the GR in recipient cells in limiting the cytokine storm caused by GvHD induction."],["dc.identifier.doi","10.18632/oncotarget.24602"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15071"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59189"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","The glucocorticoid receptor in recipient cells keeps cytokine secretion in acute graft-versus-host disease at bay"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Schneider, Constanze"],["dc.contributor.author","Thomas, Dominique"],["dc.contributor.author","Knecht, Kirsten M."],["dc.contributor.author","Buzovetsky, Olga"],["dc.contributor.author","Kaderali, Lars"],["dc.contributor.author","Schliemann, Christoph"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Angenendt, Linus"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Rothenburger, Tamara"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Scheich, Sebastian"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Wilke, Anne"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Michaelis, Martin"],["dc.contributor.author","Ferreirós, Nerea"],["dc.contributor.author","Geisslinger, Gerd"],["dc.contributor.author","Xiong, Yong"],["dc.contributor.author","Keppler, Oliver T."],["dc.contributor.author","Cinatl, Jindrich"],["dc.date.accessioned","2019-11-25T13:37:34Z"],["dc.date.accessioned","2021-10-27T13:21:34Z"],["dc.date.available","2019-11-25T13:37:34Z"],["dc.date.available","2021-10-27T13:21:34Z"],["dc.date.issued","2019"],["dc.description.abstract","Hypomethylating agents decitabine and azacytidine are regarded as interchangeable in the treatment of acute myeloid leukemia (AML). However, their mechanisms of action remain incompletely understood, and predictive biomarkers for HMA efficacy are lacking. Here, we show that the bioactive metabolite decitabine triphosphate, but not azacytidine triphosphate, functions as activator and substrate of the triphosphohydrolase SAMHD1 and is subject to SAMHD1-mediated inactivation. Retrospective immunohistochemical analysis of bone marrow specimens from AML patients at diagnosis revealed that SAMHD1 expression in leukemic cells inversely correlates with clinical response to decitabine, but not to azacytidine. SAMHD1 ablation increases the antileukemic activity of decitabine in AML cell lines, primary leukemic blasts, and xenograft models. AML cells acquire resistance to decitabine partly by SAMHD1 up-regulation. Together, our data suggest that SAMHD1 is a biomarker for the stratified use of hypomethylating agents in AML patients and a potential target for the treatment of decitabine-resistant leukemia."],["dc.identifier.doi","10.1038/s41467-019-11413-4"],["dc.identifier.pmid","31375673"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16724"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92032"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2041-1723"],["dc.relation.issn","2041-1723"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Selective inactivation of hypomethylating agents by SAMHD1 provides a rationale for therapeutic stratification in AML"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0190846"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Meers, Garrit K."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2019-07-09T11:45:08Z"],["dc.date.available","2019-07-09T11:45:08Z"],["dc.date.issued","2018"],["dc.description.abstract","Inflammatory bowel disease (IBD) is a highly prevalent intestinal disorder for which no cure exists. Currently, the standard first-line treatment of IBD consists of systemic glucocorticoid (GC) application, even though therapy can be complicated by unresponsiveness or adverse effects. In view of the importance of macrophages and neutrophils for the pathogenesis of IBD we set out to define the relevance of these cell types as targets of GC using the mouse model of DSS-induced colitis. We found that the disease did not resolve in GRlysM mice lacking the GC receptor (GR) in myeloid cells after removal of the chemical insult. While clinical symptoms and tissue damage in the colon ameliorated again in GRflox mice, the disease further aggravated in GRlysM littermates. The observed difference coincided with an increased abundance of macrophages in inflammatory infiltrates in the colon of mutant mice whereas neutrophil and T cell numbers were similar. Concomitantly, systemic IL-6 secretion and mRNA levels of pro-inflammatory cytokines in the colon were elevated in GRlysM mice and gene expression of scavenger receptors and IL-10 was diminished. Taken together, our results reveal an important role of myeloid cells as targets of GC in DSS-induced colitis and probably in IBD in humans as well."],["dc.identifier.doi","10.1371/journal.pone.0190846"],["dc.identifier.pmid","29324769"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59164"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Colitis"],["dc.subject.mesh","Colon"],["dc.subject.mesh","Dextran Sulfate"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Interleukin-10"],["dc.subject.mesh","Interleukin-6"],["dc.subject.mesh","Intestinal Mucosa"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Myeloid Cells"],["dc.subject.mesh","RNA, Messenger"],["dc.subject.mesh","Receptors, Glucocorticoid"],["dc.title","Impaired resolution of DSS-induced colitis in mice lacking the glucocorticoid receptor in myeloid cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3170"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","3183"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Blazquez, Raquel"],["dc.contributor.author","Rietkötter, Eva"],["dc.contributor.author","Wenske, Britta"],["dc.contributor.author","Wlochowitz, Darius"],["dc.contributor.author","Sparrer, Daniela"],["dc.contributor.author","Vollmer, Elena"],["dc.contributor.author","Müller, Gunnar"],["dc.contributor.author","Seegerer, Julia"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Barrantes‐Freer, Alonso"],["dc.contributor.author","Stange, Lena"],["dc.contributor.author","Utpatel, Kirsten"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Reimelt, Christian"],["dc.contributor.author","Hackl, Christina"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Büyüktas, Deram"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Balkenhol, Marko"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Krahn, Michael P."],["dc.contributor.author","Proescholdt, Martin A."],["dc.contributor.author","Riemenschneider, Markus J."],["dc.contributor.author","Evert, Matthias"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Klein, Chistoph A."],["dc.contributor.author","Hanisch, Uwe K."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-12-09T11:26:05Z"],["dc.date.accessioned","2021-10-27T13:21:49Z"],["dc.date.available","2019-12-09T11:26:05Z"],["dc.date.available","2021-10-27T13:21:49Z"],["dc.date.issued","2020"],["dc.description.abstract","More than half of all brain metastases show infiltrating rather than displacing growth at the macro-metastasis/organ parenchyma interface (MMPI), a finding associated with shorter survival. The lymphoid enhancer-binding factor-1 (LEF1) is an epithelial-mesenchymal transition (EMT) transcription factor that is commonly overexpressed in brain-colonizing cancer cells. Here, we overexpressed LEF1 in an in vivo breast cancer brain colonization model. It shortened survival, albeit without engaging EMT at the MMPI. By differential proteome analysis, we identified a novel function of LEF1 as a regulator of the glutathione (GSH) system, the principal cellular redox buffer. LEF1 overexpression also conferred resistance against therapeutic GSH depletion during brain colonization and improved management of intracellular ROS. We conclude that besides EMT, LEF1 facilitates metastasis by improving the antioxidative capacity of epithelial breast cancer cells, in particular during colonization of the brain parenchyma."],["dc.identifier.doi","10.1002/ijc.32742"],["dc.identifier.eissn","1097-0215"],["dc.identifier.issn","0020-7136"],["dc.identifier.pmid","31626715"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92047"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1097-0215"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]